The search for antiarrhythmic drugs among agents which act to augment cardiac contractility merits intensive work. We have demonstrated that prostaglandins E1 and E2 act to prevent ouabain-induced toxicity in the cat. The present research will examine the interaction of a number of different prostaglandins and digitalis materials on cardiac contractile force, cardiac output and the development of ventricular rhythm disorders. In addition, the effect of prostaglandins on ventricular fibrillation threshold will be studied in the normal, neurally deprived and ischemic heart. The present work will attempt to define the most promising antiarrhythmic compounds among the available prostaglandins and to systematically document the optimum route and rate of administration needed to provide the best antiarrhythmic action.